Dead Cells Hile Pc
Agnella Caamano
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dead cells hile pc
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While the coffeeshop rumor mills were active this past week with talk of "a lot" of corn planting going in areas of the state, in reality very little planting actually occurred (USDA Weekly Crop Progress, 13 Apr 2020). If you believe the estimates, only about 1% of the Indiana's corn crop had been planted as of 12 April. Nevertheless, based on USDA prospective planting estimates on 31 March, that would equal about 58,000 acres statewide out of the intended 5.8 million acres.
While farmers are free to plant corn whenever they choose to do do, there are risks associated with "early" planting (Nielsen, 2020). The primary risk is that associated with "cold" soil temperatures. Soils that hover around 50 degrees (F) for days or longer after planting delay germination and slow emergence of the young seedlings. More importantly, soil temperatures lower than about 50F increase the risk of "imbibitional chilling" injury to germinating seeds.
Herein lies the concern with fields that were planted during the past week, especially in central and northern Indiana. Soil temperatures at the 4-inch depth began a precipitous drop last Thursday (9 April) that accelerated over the weekend through at least today (16 April). An example of this decrease in soil temperatures is shown in Fig. 1 for the Agronomy Farm, near West Lafayette in west-central Indiana, where daily minimum soil temperatures have ranged from the 40s F down to the 30s F.
"Imbibition" refers to the initial uptake of water by seed during the first 24 to 48 hours after being planted into moist soil. The resulting rehydration causes the seed to swell and the germination process to begin. Imbibition occurs naturally, with no physiological processes involved (e.g., dry wood will imbibe water). It also occurs whether soils are cold or warm and therein lies the potential for "imbibitional chilling" injury.
When the seed swells as it rehydrates, its internal cell membrane structure is damaged. When seeds (and soil) are warm, the membrane damage is quickly repaired by the physiological activity associated with germination and "life goes on" normally. When seeds (and soil) are cold, their cell membranes are less elastic, the cell membrane damage due to swelling is more severe, and the physiological repair of the damage is slowed or stopped. Left unrepaired, this damage to cell membranes and the subsequent leakage of cell contents can result in death of the seed.
Past research on the nature and causes of imbibitional chilling injury to seed does not clearly identify the environmental conditions "in the real world" that result in a high probability of the problem. The literature implies that soil temperatures simply lower than 50F are a key factor. It is not clear from past research whether the injury can occur with only a few hours of exposure to sub-50F soil temperatures or whether it requires lengthier exposure to cold temperatures. What is known is that this type of chilling injury is most likely to occur during the first 24 to 48 hours after planting seed into moist soil because that is when imbibition (and corresponding seed swelling) occurs.
Identifying and the diagnosing the problem in the field is often challenging for several reasons. First of all, germination and emergence of corn in cold soils will naturally be slow. The first visual indicator of germination (other than the seed swelling) is the appearance of the radicle root between 35 and 60 Growing Degree Days (GDD) after planting (Nielsen, 2019).
When soil temperatures hover around 50F for days or longer after planting, accumulating 35 to 60 GDD may take 1 to 2 weeks. Initially, dead seed due to imbibitional chilling injury do not look much different than live seed taking their normal "sweet time" to germinate in cold soils. However, once 60 GDD or more have accumulated, then seed that seems to be "dormant" compared to others that exhibit radicle roots, coleoptiles, and lateral seminal roots may well be the result of imbibitional chilling injury. Sometimes, instead of immediate cessation of the germination process (i.e., "dormant" seed symptom), the radicle root and coleoptile emerge from the seed coat before ceasing further development (Fig. 2).
Another challenge in diagnosing imbibitional chilling injury as the cause of poor stands of corn is that eventually the dead seed or seed that germinated but simply ceased further development will naturally begin to decompose. Consequently, if you wait too long to investigate a problem field, you might be tempted to diagnose seed or seedling disease as the cause of the poor stand.
Daily, or hourly, soil temperature records coupled with knowledge of a field's planting date are useful for "pointing the finger" at imbibitional chilling injury. Because imbibition occurs within the first 24 to 48 hours after planting into moist soil, one can imagine that timing of planting relative to the onset of several days of cold soil temperatures influences the risk of imbibitional chilling injury. Anecdotal stories abound in the coffeeshops about fields planted 3 days ahead of a cold snap emerging just fine... fields planted 2 days ahead of the cold snap experiencing some emergence problems... fields planted 1 day ahead of the cold snap having more problems... and fields planted the day of the cold snap having major problems.
Bottom Line: If you were among the ambitious souls who chose to plant more than a few acres of corn during the past 7 days or so, I encourage you to scout those fields over the next week or so to assess the success of germination and emergence. Emergence success is usually lower for early planting versus later, warmer, planting. However, the risk exists for unusually lower emergence success this year because of the unusually low soil temperatures of the past week.
An Interesting Question: Bill Cox, Extension Corn Specialist at Cornell University in New York, raised a question several years ago about whether modern hybrids are still susceptible to imbibitional chilling injury (Cox, 2014). Based on a small set of trial data from Cornell's Aurora Research Farm in Cayuga County NY, Bill concluded the answer was "maybe not" and that "...the timing of the adverse conditions would have to be so unique and so time-dependent in the first 48 hours after planting that it may not be worth worrying about".
I admit that Bill may have a point. I have not encountered many clear-cut examples of imbibitional chilling injury in all the years I have worked with corn in Indiana, as exemplified by the fact that I have so few photos of the problem in my image collection of various corn problems. Nevertheless, the risk for imbibitional chilling injury with cold soils is real. That risk plus the indisputable fact that that cold soils are simply not conducive to desirable rapid germination and emergence of corn should always be weighed when choosing to plant corn early in soils that are cold or likely to become cold.
Both can present early in the post-op period and share similar symptoms such as decreased visual acuity, redness and pain. The pain is usually mild with TASS but is often a deep ocular pain with endophthalmitis. Signs can be similar as well, including hypopyon, anterior chamber reaction such as fibrin formation and corneal edema. Endophthalmitis may show a vitritis and loss of red reflex.
TASS occurs when toxic substances enter the anterior chamber and cause a sterile, noninfectious postoperative inflammatory response. Signs and symptoms of TASS present within 12 to 24 hours of cataract or refractive surgery and can include hypopyon, fibrin formation in the anterior chamber, corneal edema, irregular pupil, decreased visual acuity, mild pain and redness. Cellular necrosis and apoptosis occur, resulting in acute postoperative inflammation. The toxic substances break down the corneal endothelial junctions, causing the viable remaining cells to spread out over the damaged area in an effort to maintain the endothelial pumping system. If the remaining functional cells are unable to compensate for the loss, it can cause permanent corneal edema. Due to its inability to regenerate and replace dead cells, the corneal endothelium is often the most damaged structure. If the trabecular meshwork is damaged as well, it can cause decreased aqueous outflow, peripheral anterior synechiae and increased intraocular pressure.2
2. Enzymes and detergents remain on cleaned instruments. This can be especially problematic with multi-specialty surgical centers that use enzymes and detergents generously to clean off tissue left on surgical instruments from several types of surgery. Any residue that remains on the instruments from this cleaning process can cause inflammation. Better education can help multispecialty surgical centers and hospitals understand that ophthalmic surgery rarely leaves tissue on instruments, and the use of these detergents and enzymes, which can be a cause of inflammation, may not be necessary.2
3. Endotoxin contamination during instrument sterilization. Even though gram-negative bacteria, which can reside in water baths and autoclave reservoirs, are killed during autoclaving, heat-resistant endotoxins from the bacteria can remain on instruments. The water used for these cleaning procedures must be changed regularly to avoid this complication.
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